Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: the Role of Noninvasive Ventilation
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Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation Claudio Terzano1, Fabio Di Stefano1, Vittoria Conti1*, Marta Di Nicola2, Gregorino Paone1, Angelo Petroianni1, Alberto Ricci1 1 Fondazione Eleonora Lorillard Spencer Cenci, Sapienza University of Rome, Rome, Italy, 2 Laboratory of Biostatistics, Department of Biomedical Science, University ‘‘G. d’Annunzio’’ of Chieti-Pescara, Chieti, Italy Abstract Background: Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Methods: Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO2 and PaCO2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Results: Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosis–metabolic alkalosis, 10/36 (27.8%) respiratory acidosis and 3/5 (60%) mixed respiratory-metabolic acidosis patients (p = 0.026), with durations of 45.169.8, 36.268.9 and 53.364.1 hours, respectively (p = 0.016). The duration of ventilation was associated with higher blood lactate (p,0.001), lower pH (p = 0.016), lower serum sodium (p = 0.014) and lower chloride (p = 0.038). Hyponatremia without hypervolemic hypochloremia occurred in 11 respiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis–metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. Conclusions: Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated. Citation: Terzano C, Di Stefano F, Conti V, Di Nicola M, Paone G, et al. (2012) Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation. PLoS ONE 7(4): e35245. doi:10.1371/journal.pone.0035245 Editor: Mauricio Rojas, University of Pittsburgh, United States of America Received October 9, 2011; Accepted March 12, 2012; Published April 23, 2012 Copyright: ß 2012 Terzano et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: The authors have no support or funding to report. Competing Interests: The authors have declared that no competing interests exist. * E-mail: [email protected] Introduction 40 mmHg, the ideal value of SID is 42 mmol/L . An increased SID causes alkalosis; a reduced SID causes acidosis. Altering SID Hypercapnic respiratory failure is a complex condition means altering the water dissociation equilibrium. This provides associated with the malfunction of various organs and systems more/less H+ for electroneutrality, with a change in [H+], and so a crucial for many physiological processes, leading to an acid-base change in pH. imbalance. Acid-base and electrolyte balance are part of the same picture Carbon dioxide (CO2) is not the only independent variable that because, for a given increase in CO2, the only way to minimize the may cause alterations in acid-base status. Total serum protein, resulting acidemia is to produce compensatory metabolic alkalosis, albumin in particular, plays an important role, as does the strong which is obtained through complex urinary ion excretion ion difference (SID), that is the difference between the strong mechanisms [2]. Thus, fluid homeostasis depends on the correct positive ions in the plasma (sodium (Na+), potassium (K+), calcium + + relationship between lung and kidney activities because they (Ca2 ), and magnesium (Mg2 )) and the strong negative ions + 2 2 regulate most of the CO2 and hydrogen (H ) concentrations in the (chloride (Cl ) and lactate (Lac )): extracellular volume, whose total solutes consist almost entirely of + 2 32 ÂÃNa ,Cl and bicarbonate ions (HCO ). { SID~ NazzKzzCa2zzMg2z {½Cl zLac{ : ð1Þ In hypoxic and hypercapnic COPD patients, fluid homeostasis is disturbed, with avid retention of sodium and water [3]. The At pH 7.4, 37uC and a partial carbon dioxide tension of increase in sodium retention by the kidneys during COPD, and PLoS ONE | www.plosone.org 1 April 2012 | Volume 7 | Issue 4 | e35245 Mixed Acid-Base Disorders in Respiratory Failure the consequent edema, may be explained in part by right heart failure (cor pulmonale) and by other pathophysiological mecha- ðÞÃTBW ½1{ðÞ140=Naz : nisms involving renal and hormonal abnormalities [3,4]. In hypercapnic COPD exacerbations, the sudden decrease in Plasma osmolality was calculated using the following equation: ventilation causes an acute respiratory acidosis or deteriorates a pre-existing chronic respiratory acidosis. Due to the high ½Glucose ½BUN prevalence of comorbidities [5] and the associated multidrug 2Na½z z z : therapies in these patients, mixed acid-base and hydro-electrolyte 18 2:8 disorders are becoming increasingly common, particularly in the Because the patients’ clinical conditions did not allow us to critically ill and elderly populations. conduct reliable pulmonary function tests, the data (FVC and This study had the following aims: to evaluate mixed acid-base, FEV1) considered for the analysis were those measured subse- hydro-electrolyte and lactate disorders in patients with hypercap- quently at a stable clinical condition (or rather when vital and gas- nic COPD exacerbation; to determine the relationship among exchange parameters improved and stabilized and patients’ these disorders, a poor response to pharmacological treatment and dyspnea was not severe enough to not allow respiratory manouvres the requirement for noninvasive ventilation (NIV); and to analyze required by lung function testing). the link between these disorders and the duration of NIV in the Initially, all patients received controlled oxygen therapy with a treatment of hypercapnic respiratory failure. Venturi mask, in order to maintain an arterial oxygen saturation (SaO2) at least $90%, and conventional treatments, including Methods nebulized bronchodilators, intravenous corticosteroids, antibiotics (if necessary) and other drugs, depending on the concomitant Ethics Statement comorbidities. NIV was initiated when controlled oxygen therapy The institutional review board for human studies (Fondazione and convientional medical treatments failed to improve the clinical Eleonora Lorillard Spencer Cenci Ethics Committee) for human conditions, or rather when respiratory distress with accessory studies approved the protocol, and written consent was obtained muscle use or abdominal paradox and tachypnea (respiratory rate from the subjects or their surrogates. .24/min) were associated with persistent arterial impairment (pH,7.35, PaCO2.45 mmHg, and PaO2/FiO2,200) despite Study design optimal pharmacological treatment and oxygen therapy [7,13]. We investigated patients consecutively hospitalized in our NIV was performed via an oronasal mask using a pressure support respiratory ward (Respiratory Diseases Unit, Policlinico Umberto turbine ventilator (Polar 2 Hackermann & Bild Ltd., Crespellano, I, Rome) for COPD exacerbation and hypercapnic respiratory Bologna, Italy) with a bi-tube connection. The pressure support, failure. Between January and April 2010, sixty-seven patients were PEEP and flow-by trigger values were adjusted to obtain a tidal consecutively hospitalized for COPD exacerbation and hypercap- volume of 6–8 ml/kg and to gain the best oxygenation and reduce nic respiratory failure. COPD and COPD exacerbation were the respiratory rate. They were modified based on the blood gas defined according to the Global Initiative for Chronic Obstructive data. Heart and respiratory rates, pH, PaO2 and PaCO2 and Lung Disease (GOLD) guidelines [6]. Hypercapnia was defined by blood lactate were checked on the 1st,2nd,6th and 24th hours after a PaCO2$45 mmHg on arterial blood gas (ABG) analysis [6]. starting NIV. Patients were excluded from this descriptive study if they had NIV was withdrawn when the clinical condition improved and concomitant pneumonia, acute lung injury (ALI) or acute stabilized, as defined by the following objective parameters: respiratory distress syndrome (ARDS), and contraindications to respiratory rate ,24/min, heart rate ,110/min, pH.7.35 and noninvasive ventilation (NIV) [7]. Patients enrolled were not SaO2.90% on FiO2,40% [14]. Patients were a priori considered necessarily at the first COPD exacerbation treated with NIV, but for invasive mechanical ventilation if the following conditions were those being on chronic NIV treatment at home were excluded. present: a worsening of arterial pH and carbon dioxide tension Comorbidities were identified on the basis of clinical records, despite correct NIV administration, an